Year: 2022
Type: editorial
Abstract: Van der Lely et al. [1] present a traditionally thorough meta-analysis considering the question of neural monitoring of central responses to lower urinary tract (LUT) function (LUT electrical sensory assessment [LUTESA]). Based on their review of a thorough and defended selection of primary literature, the authors conclude that the extracted studies show that LUTESA is a feasible and safe approach by which to evaluate the sensitivity of LUT afferents in healthy subjects and patients, as well as to obtain information on nerve fibre integrity and conduction velocity. This is not supported, however, by the reviewed literature (and, therefore, quite likely not by any available clinical research). Current perception testing (CPT), in particular, and probably also sensory evoked potentials (SEP), report perceptions generated by higher cortical activity/functions, which, although dependent to a large degree on urethral and bladder dorsal root ganglion afferent neuronal activity, are not solely determined by these inputs. Brainstem/bladder and cognitive/perceptual feedback/forward loops are among the confounders that probably modulate the signalling; it is therefore not surprising that ‘fixed’ lesions, such as neuropathy/injury, yield expected results but other factors, such as aging and non-neurogenic (i.e. identifiable neuronal lesion) symptom complexes, yield more inconsistent results. What the authors have nicely shown is that reliable, consistent and probably robust signals can be obtained, which are likely to contain significant coding relating to perceptions of LUT dysfunction. The nature of these signals appears to be highly dependent on technique/generative details, consistent with the high risk of bias observed. This is not surprising; however, the meaning of those signals is not revealed by this analysis, despite the temptation to make such equations in both clinical research and eventually in practice. The disconnect between the neuro-/cognitive science and the clinical experience is the result of the simplistic and imprecise assumption that traditional urodynamic-based models of signalling/dysfunction are complete and accurately reflect the neurocognitive physiology of bladder control. Fundamentally, the authors (both of the present paper and its sources) posit that a lack of objective (patho)physiological data is a clinical diagnostic knowledge gap. If, as postulated, LUT CPT/SEP can address that gap, it is possible that long-held traditions about ‘pathology’ will require reconsideration. Much more could be gleaned from future studies by reframing the question. The authors have started with standard urodynamic, International Continence Society (ICS) terminology-defined modelling of non-fixed-lesion LUT dysfunction/symptoms, which they correctly acknowledge early on is a subjective approach. Several studies, at least going back to an early report of videourodynamics [2], note the lack of reliable linkage of urodynamic observations and patient reports, a fact well understood by any clinician who personally conducts and interprets urodynamic evaluations. The utility of LUTESA, both in revealing deeper understandings of pathological/physiological processes and possibly also for clinical application, might be greatly enhanced in future studies by categorization of test results primarily according to CPT or SEP findings, based on normalized responses to a given technique (e.g. CPT waveform/frequency/administration techniques), independent of pre-existing knowledge of symptoms, observations, and/or urodynamic categorizations disease/injury/symptom/dysfunction as defined by accepted ICS terminologies. Once this new categorization is completed, correlations of LUT CPT/SEP findings with organic and symptom-based pathologies might then be sought. How the strength of those correlations varies with technical details could potentially provide important insight into both physiology and the clinical utility of technical variations. Finally, these human data should be considered in the context of available animal data and might be used to guide future laboratory investigation. While animal data cannot address the uniquely human cortical/cognitive aspects of LUT perception and control, the volume-derived signal generation, brainstem responsiveness, and brainstem-switching mechanisms and robustness are both pertinent to cortical responses and are topics of ongoing animal research. Overall, although this analysis must be read with a degree of circumspection, and in my opinion cannot be used to support clinical use of LUTESA, the authors have provided a good overview of what is known. Rather than being useful to guide clinical practice, their findings will be much more valuable as guidance for future research methods and approaches. These technologies may hold promise to free pathophysiological modelling of LUT dysfunction/symptoms from the long-standard and canonic linkage to a bladder/detrusor/sphincteric focus, an approach that after more than a century of research still cannot offer routinely safe, effective and durable curative solutions to these common clinical problems. None declared. [Correction added on 06 Aug 2022 after first online publication: Reference 1 has been updated in this version.]
Source: British Journal of Urology
DOI: 10.1111/bju.15584
Author: Phillip P. Smith
Institutions: University of Connecticut, UConn Health
Language: English
Subfield: Urology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W4285493134